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Stroke, Heart Attack Damage Could Be Mitigated via Mimicry of Good Cholesterol

저자:   업로드:2017-08-18  조회수:

    It may be a caricature, but it is recognized by ailing blood vessels, which respond by moving closer to a picture of cardiovascular health. The “it” is an artificial protein called ApoM-Fc that mimics apolipoprotein M (ApoM), a natural protein that is a component of high-density lipoprotein (HDL), or “good cholesterol.” ApoM-Fc performs better than synthetically derived ApoM, which is expensive to produce and has just a 15-minute half-life in the body’s bloodstream. In tests on mice, ApoM-Fc lowered blood pressure and alleviated tissue damage caused by stroke, heart attack, and other cardiovascular diseases.


    ApoM-Fc, like ApoM, ferries S1P, or sphingosine-1-phosphate, particles through the bloodstream to endothelial cells, which line the blood vessels and are studded with S1P receptors. When these receptors recognize S1P, and bind them, endothelial cells work to suppress inflammation, thereby promoting cardiovascular health. Unfortunately, S1P doesn’t work on its own. It needs a chaperone, a sort of carrier.


    The artificial S1P carrier was engineered by scientists based at Boston Children's Hospital Vascular Biology Program. These scientists, led by Timothy Hla, Ph.D., showed that their novel protein could trigger increased S1P receptor activity and recover blood vessel health.


    Details of the scientists’ work appeared August 15 in the journal Science Signaling, in an article entitled “An Engineered S1P Chaperone Attenuates Hypertension and Ischemic Injury.” The article noted that while HDL is known to alleviate endocardial dysfunction, globally increasing HDL abundance is not beneficial, suggesting that “specific HDL species mediate protective effects.” The article also indicated that the Boston Children’s team decided to focus on ApoM-positive HDL.




    “We report the development of a soluble carrier for S1P, ApoM-Fc, which activated S1P receptors in a sustained manner and promoted endothelial function,” wrote the article’s authors. “ApoM-Fc administration reduced blood pressure in hypertensive mice, attenuated myocardial damage after ischemia/reperfusion injury, and reduced brain infarct volume in the middle cerebral artery occlusion model of stroke.”


    The authors also emphasized that ApoM-Fc did not modulate circulating lymphocyte numbers, suggesting that it specifically activated endothelial S1P receptors.


    "HDL carries a protein called ApoM, which in turn attracts and binds S1P in its cargo," explained Dr. Hla, the senior author on the new paper. "Together, this trio activate

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